The Effects of Intentional Changes of Brain Temperature on The Experimental Brain Contusion

有意改变脑温度对实验性脑挫裂伤的影响

• 批准号: 07671499
• 负责人: YAMAURA Akira
• 金额: $ 1.47万
• 依托单位: Chiba University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07671499/
• 关键词: experimental brain injury; intentional changes of brain temperature; heat shock protein; hypothermia; immunohistochemistry; glial response; 実験的脳挫創

In this project, we investigated the effects of intentional changes of brain temperature on the experimental brain contusion. Firstly as a preliminary study, in 1995, we evaluated the immunohistochemical expression of 72 kDa heat shock protein (HSP72) as a marker of neuronal damage. Adult male rats were subjected to a lateral fluid percussive injury. Injured rats were divided into two groups ; normothermic group (37.0-37.5ﾟC) and hypothermic group (30.0-31.5ﾟC). The immunohistochemical evaluation was performed at 24,48, and 72 hours after injury. The results showd that HSP72-positive neurons were observed most prominently at 24 hours in both groups but their numbers in hypothermic group were significantly less than those in normothermic group. This preliminary study suggested that the protective effects of moderate hypothermia on the injured brain. According to these results, in 1996, we made a plan to evaluate the effects of intentional changes of brain temperature on blood-brain barrier (BBB) disruption and glial response. However, after the completion of the preliminary study in 1995, some problems which disturbed the next plan occured : 1) The breakdown of fluid percussive injury device and vibratome. 2) Unexpected non-specific background staining in immunohistochemisty. 3) Technical problems such as new cooling-heating method and insertion of epidural thermosenser into posterior fossa. 4) The possibility of difference in brain injury formation between old (1995) and new (1996) injury model. As a result, among 22 treated rats, we could evaluate only three rats (34ﾟC group=2,37ﾟC group=1) concerning to expression of HSP72 and glial response at 24 hours after injury. The results showed that there were no obvious effects of mild hypothermia (34ﾟC) on expression of HSP72 and microglial activation, whereas astrocytic responses were seemd to decrease in mild hypothermic group.

在本课题中，我们研究了故意改变脑温度对实验性脑挫伤的影响。首先，作为初步研究，我们在1995年评价了72 kDa热休克蛋白(HSP72)的免疫组织化学表达作为神经元损伤的标志。成年雄性大鼠采用侧向液压冲击伤模型。损伤大鼠分为常温组(37.0~37.5ﾟC)和亚低温组(30.0~31.5ﾟC)。分别于伤后24、48、72h进行免疫组织化学检测。结果表明，两组大鼠脑内HSP72阳性神经元均在24小时出现，但亚低温组阳性神经元数量明显少于常温组。这一初步研究提示，亚低温对脑损伤有保护作用。根据这些结果，我们在1996年制定了一项计划，以评估故意改变脑温度对血脑屏障(BBB)破坏和神经胶质反应的影响。然而，在1995年初步研究完成后，出现了一些困扰下一步计划的问题：1)液压冲击伤装置和振动器故障。2)免疫组织化学中意外的非特异性背景染色。3)新的冷热方法、硬膜外温度传感器植入后颅窝等技术问题。4)旧(1995)和新(1996)脑损伤模型在脑损伤形成方面存在差异的可能性。结果表明，在22只治疗大鼠中，仅有3只大鼠(34ﾟC组=2只，37ﾟC组=1只)可以评估HSP72的表达和伤后24小时的神经胶质反应。结果表明，亚低温(34ﾟC)对HSP72的表达和小胶质细胞的激活无明显影响，而星形胶质细胞的反应似乎有所减少。